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Endorsements for Digestive Wellness 4th Edition
Stock Image. Published by Thundersnow Interactive, United States, New Condition: New Soft cover. Save for Later. About this Item Language: English. Brand new Book. About this title Synopsis: Karen DeFelice follows up her two previous works on the subject of enzymes with this book, a look at enzyme therapy which updates the reader on the latest developments in the field and makes the information practical for everyday use.
Store Description Book Depository is an international bookseller. We ship our books to over countries around the globe and we are always looking to add more countries to the list. Corey et al. Fitzsimmons et al. However, this represents a small case series published in NEJM in , which were not biopsy proven with very few cases reported since then. Factors related to CF, including thick intestinal secretions, dosing of PERT, and agents in the enteric coating of the pancrelipase preparations may be the precipitating factors causing this complication [ 18 ].
Factors that contribute to EPI following pancreatic surgery are a decrease in pancreatic tissue volume, extensive denervation following lymph node dissection, and surgically altered anatomy [ 6 ]. Conditions such as pancreatic cancer, intraductal papillary mucinous neoplasms, premalignant mucinous cystic lesions, and benign tumors of the pancreas may all lead to EPI via obstruction of the pancreatic duct.
The degree of EPI following pancreatic surgery is dependent on the extent of pancreatic resection combined with the degree of residual pancreatic parenchymal function with full manifestation of EPI seen following a total pancreatectomy [ 20 , 21 ]. The mechanism of EPI in patients undergoing a Whipple procedure may be related to a mistiming of secreted endogenous pancreatic enzymes mixing with chyme.
In addition, Halloran et al. These patients with newly developed EPI, however, did have a tendency towards poorer quality of life. Celiac disease is a chronic inflammatory intestinal disorder that may occur in genetically predisposed people triggered by the ingestion of gluten. In celiac disease, although exocrine pancreatic function is intrinsically normal, reduced levels of cholecystokinin release as a result of the duodenal villous atrophy, accounts for impaired gall bladder contraction and reduced exocrine pancreatic secretion [ 32 , 33 ].
The term islet-acinar axis has been used to describe the endocrine-exocrine relationship within the pancreas, whereby there is a vascular and physiologic interaction between these different cell types [ 34 ]. Pathophysiologically, diabetes mellitus can predispose to EPI and, conversely, longstanding EPI can be associated with diabetes [ 35 — 39 ]. In diabetes, there are several possible causes which can account for EPI — the lack of the trophic action of insulin and potentially of glucagon and somatostatin on acinar cells, autoimmune damage of islet cells, causing destruction of both endocrine and exocrine tissue, and decreased exocrine pancreatic secretion as a complication of diabetic neuropathy [ 36 , 37 ].
In addition, a recent article by Soave et al. Based on the study by Lebenthal and Lee [ 40 ] indicating that the duodenal fluid of newborns and infants contained no amylase and negligible lipase at least for the first month of life, all healthy term infants are exocrine pancreatic insufficient. Normally, this is compensated for by amylase and lipase present in breastmilk. However, in formula-fed infants, EPI would be expected. In fact, a recent study by Martin et al. Thus, all infants, both term and preterm, represent the largest population of individuals with EPI.
The clinical implications of developmental pancreatic insufficiency in non-breast-fed infants is unknown, but may play a role in early nutrient deficits in critically ill newborns such as the preterm infant.
Expert opinion: Routinely checking for EPI in patients with chronic diarrhea, using fecal elastase, is unreliable in the absence of testing a formed stool. A multitude of tests for EPI have been developed over the past several decades and classified as direct versus indirect measures of exocrine pancreatic function.
However, many of these have poor sensitivity or specificity e. Unfortunately, this test is time-consuming and not easily tolerated due to bloating, abdominal discomfort, flatulence, and worsening steatorrhea. Additionally, errors can occur in stool collections and recording of fat intake [ 42 ].
The pancreas produces pancreatic elastase 1, which is a highly stable enzyme during intestinal transit [ 44 ]. This proteolytic enzyme can be measured in a fecal sample by an enzyme-linked immunosorbent assay [ 45 , 46 ]. Because pancreatic elastase is highly stable during intestinal transit, the fecal concentration correlates well with exocrine pancreatic secretion [ 45 ].
Diagnostic testing using fecal elastase has some advantages over other tests because it does not require a timed stool collection or special diet, has a high negative predictive value, and has a high sensitivity in moderate to severe EPI when formed stools are analyzed [ 8 , 42 , 47 , 48 ].
Since fecal elastase is measured as a concentration in stool, watery stools will almost invariably result in low elastase values being measured and thus this non-invasive, pancreatic function test should be performed in a clinical setting where EPI is suspected and a formed stool can be analyzed. This has replaced the more cumbersome hour fecal fat test.
In addition, PERTs do not have to be stopped for fecal elastase testing since the porcine enzymes do not cross react with the human fecal elastase antibody.
Myth: PERT should be started at the lowest dose available and taken any time before a meal and at bedtime. Fat malabsorption is the predominant cause of the symptoms of pancreatic steatorrhea resulting in weight loss as well as deficiencies of fat-soluble vitamins A, D, E, and K.
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In patients with chronic pancreatitis, a low fat diet has been the recommendation in order to minimize the pain of this disease and, in conjunction with PERT, to effectively treat steatorrhea. However, in patients with CF, a high fat diet in conjunction with increased amounts of PERTs has been shown to improve the associated CF lung disease and thus low fat diets are no longer advocated in this disease. Consulting a dietitian is helpful to assess nutritional adequacy [ 55 ]. In addition, smoking has been proven to be a risk factor in acute pancreatitis, chronic pancreatitis, pancreatic cancer [ 56 ], and to be associated with reduced exocrine pancreatic function [ 57 ].
Therefore, smoking and alcohol cessation is recommended in EPI due to chronic pancreatitis. The elimination of malabsorption, reduction of maldigestion-related symptoms, and the prevention of malnutrition-related morbidity and mortality is the goal for PERT [ 55 ].
Prior to , pancreatic enzymes were not FDA regulated and had variable consistency of activity. It should be noted that the clinical trials were relatively small less than 40 subjects and tested in subjects who were known to respond to PERTs. All pancreatic enzyme preparations are extracts from porcine pancreas pancrelipase and are available in preparations encapsulated in mini-microspheres or microtablets, which vary in particle size and pH-related release kinetics [ 58 ].
Enteric-coated pancreatic microspheres are designed to be acid resistant and pH-sensitive to protect lipase from denaturation by gastric acid. The use of acid-suppression medications can increase gastric pH levels and theoretically improve the efficacy of PERT and decrease EPI symptoms [ 61 , 62 ]. Current data may suggest a trial of acid blockers in patients with CF who have refractory steatorrhea [ 61 — 65 ]. However, a recent retrospective study demonstrated no improvement of the coefficient of fat absorption hour fecal fat test when using a proton pump inhibitor in pediatric patients with CF [ 66 ].
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Uncoated exogenous pancreatic enzymes, such as Viokase Aptalis Pharma , are thought to mix well with intragastric nutrients and rapidly release high duodenal lipase amounts for fat digestion [ 58 ]. The addition of acid-suppression medications is required to prevent degradation of non-enteric coated pancreatic enzymes [ 58 ]. Only non-enteric pancreatic enzymes have been shown to improve the pain in a subset of patients with chronic pancreatitis.
The use of unprotected exogenous enzymes in combination with enteric-coated enzymes has previously been recommended for the treatment of refractory EPI [ 58 , 67 ]; however, Kalnins et al. Dosing and frequency of administration are difficult aspects of PERT treatment since different enteric-coated microspheres are not bioequivalent in vitro [ 69 — 71 ], and there are not enough clinical studies between preparations to define in vivo bioavailability.
Several countries have recommended different doses of PERT. Unfortunately, the evidence for these recommendations is relatively weak as emphasized by The Australasian Pancreatic Club in their recent study on the management of pancreatic exocrine insufficiency [ 72 ]. In addition, a study from the Netherlands by Sikkens et al. These differences in recommendations demonstrate the significant confusion over dosing and administration amongst medical practitioners.
Likewise, there is no consensus over frequency of PERT administration. In , DiMagno et al. In addition, a recent randomized three-way crossover study of 24 patients using 40, lipase units per meal compared three different administration schedules with PERT before meals, during meals, or after meals using the 13 C-MTG breath test to measure fat absorption [ 79 ].
Thus, no statistically significant differences were found between different administration schedules, however, they did recommend giving PERT during or after meals. In a patient with suspected EPI with a known history of pancreatic disease, empiric therapy with PERTs may be indicated without formal testing. A clear response would be both diagnostic for EPI as well as therapeutic.
Treatment strategies for lack of response to pancreatic enzyme replacement therapy PERT. PERT should be taken with the first bite of a meal and consider adding extra enzymes during or towards the end of the meal.
The rationale for taking pancreatic enzymes throughout the meal is to mimic the action of our own endogenous pancreatic enzymes, where secretion from the gland occurs throughout a meal. These therapies have improved signs and symptoms related to EPI such as steatorrhea and abdominal discomfort, weight loss, malnutrition, and possibly even quality of life.
However, there is still much confusion amongst medical practitioners over the best diagnostic approach as well as dosing and administration of PERT. Many countries have developed different guidelines regarding dosing and administration of PERT, calling out for a consensus and a practical guide for the diagnosis and treatment of EPI using exogenous pancreatic enzymes.
In addition, evidence supports that patients are being undertreated with PERT and may potentially benefit from more adequate therapy. There are two areas that need emphasis. Over the last decade, there has been a change in diagnostic approach for EPI from the unreliable qualitative stool test and the cumbersome hour fecal fat collection, to the more sensitive, but less specific, fecal elastase test, especially in patients with mild to moderate EPI. Many physicians do not realize the need to have formed stools analyzed and thus, in chronic diarrhea, this may be problematic.
Ultimately, what is critical is the early diagnosis and optimization of treatment of EPI. Second, there must be optimization of the currently available therapies for EPI. The existing studies vary on recommendations for dosing of exogenous pancreatic enzymes ranging from 25, to 80, lipase units per main meal, and there is uncertainty about administration of PERT before, during, or after the meal. In addition, the treatment goals differ from reducing pancreatic steatorrhea and elimination of maldigestion and malabsorption, to the prevention of malnutrition-related morbidity and mortality.
This is all complicated by the myriad of pancreatic enzyme formulations at a wide array of dosing strengths. Thus, it is not surprising that confusion amongst physicians exists over the optimal dosage, administration schedule, and what to aim for in PERT. MRS, Dr. SDF, and Dr. CRM contributed equally to the review of the literature on EPI and writing and revising of the manuscript.
Pancreas Enzyme - an overview | ScienceDirect Topics
All authors read and approved the final manuscript. He is Director of The Pancreas Center and is a worldwide leading expert on pancreatic disease and cystic fibrosis. She is an international expert on fatty acids and nutrition in preterm infants.